Structural analysis of arteriolar and myocardial remodelling in the subendocardial region of patients with hypertensive heart disease and hypertrophic cardiomyopathy

Mundhenke, M.; Schwartzkopff, B.; Strauer, Bodo E.

doi:10.1007/s004280050098

Cited by 60 publications

(54 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As previously found by others, 6,12,30,31 we did observe that all patients studied showed an excessive collagen accumulation into the myocardium. Furthermore, we found that serum PIP correlates directly with myocardial CVF in hypertensives.…”

Section: Pathophysiological Meaningsupporting

confidence: 73%

Serum Carboxy-Terminal Propeptide of Procollagen Type I Is a Marker of Myocardial Fibrosis in Hypertensive Heart Disease

Querejeta¹,

Varo²,

López³

et al. 2000

Circulation

327

228

View full text Add to dashboard Cite

Background-This study was designed to investigate whether the serum concentration of the carboxy-terminal propeptide of procollagen type I (PIP), a marker of collagen type I synthesis, is related to myocardial fibrosis in hypertensive patients. Methods and Results-The study was performed in 26 patients with essential hypertension in which ischemic cardiomyopathy was excluded after a complete medical workup. Right septal endomyocardial biopsies were performed in hypertensive patients to quantify collagen content. Collagen volume fraction (CVF) was determined on picrosirius red-stained sections with an automated image analysis system. The serum concentration of PIP was measured by specific radioimmunoassay. Compared with normotensives, both serum PIP and CVF were increased (PϽ0.001) in hypertensives. A direct correlation was found between CVF and serum PIP (rϭ0.471, PϽ0.02) in all hypertensives. Histological analysis revealed the presence of 2 subgroups of patients: 8 with severe fibrosis and 18 with nonsevere fibrosis. Serum PIP was higher (PϽ0.05) in patients with severe fibrosis than in patients with nonsevere fibrosis. Using receiver operating characteristic curves, we observed that a cutoff of 127 g/L for PIP provided 78% specificity and 75% sensitivity for predicting severe fibrosis with a relative risk of 4.80 (95% CI, 1.19 to 19.30). Conclusions-These results show a strong correlation between myocardial collagen content and the serum concentration of PIP in essential hypertension. Although preliminary, these findings suggest that the determination of PIP may be an easy and reliable method for the screening and diagnosis of severe myocardial fibrosis associated with arterial hypertension.

show abstract

Section: Pathophysiological Meaningsupporting

confidence: 73%

Serum Carboxy-Terminal Propeptide of Procollagen Type I Is a Marker of Myocardial Fibrosis in Hypertensive Heart Disease

Querejeta¹,

Varo²,

López³

et al. 2000

Circulation

327

228

View full text Add to dashboard Cite

show abstract

“…20 In previous studies, we reported thickening of the media wall and increased periarteriolar fibrosis in hypertensive patients compared with normotensive control subjects. 15 In the present study, we observed a slight, but not significant, reduction in the media cross-sectional area after ACE inhibitor treatment. In addition to the regression of media hypertrophy, angiogenesis with an increase in the number of parallel resistance vessels or a re-remodeling of preexisting material in the vessel wall, causing larger lumen diameter after maximal vasodilatation, can result in an improved coronary reserve.…”

Section: Coronary Blood Flow Measurementssupporting

confidence: 55%

“…Reproducibility of morphometric data has been extensively investigated, and measurements were made according to a previously reported protocol from our group. 5,15,16 …”

Section: Morphological Investigationmentioning

confidence: 99%

Repair of Coronary Arterioles After Treatment With Perindopril in Hypertensive Heart Disease

et al. 2000

Self Cite

View full text Add to dashboard Cite

Abstract-In hypertensive heart disease, no data are available on the repair of coronary resistance vessels in patients after long-term ACE inhibitor treatment. Fourteen patients with essential hypertension were studied with coronary flow reserve and with transvenous endomyocardial biopsy before and after 12 months of antihypertensive treatment with perindopril (4 to 8 mg/d, mean 5.9Ϯ2.3 mg/d). Left ventricular muscle mass index decreased by 11% (from 145Ϯ41 to 128Ϯ36 g/m 2 , Pϭ0.04). Maximal coronary blood flow was increased by 54% (from 170Ϯ46 to 263Ϯ142 mL ⅐ min Ϫ1 ⅐ 100 g Ϫ1 , Pϭ0.001), and minimal coronary vascular resistance was diminished by 33% (from 0.67Ϯ0.21 to 0.45Ϯ0.19 mm Hg ⅐ min ⅐ 100 g ⅐ mL Ϫ1 , Pϭ0.001); consequently, coronary reserve increased by 67% from 2.1Ϯ0.6 to 3.5Ϯ1.9 (Pϭ0.001). Structural analysis revealed regression of periarteriolar collagen area by 54% (from 558Ϯ270 to 260Ϯ173 m 2 , Pϭ0.04) and of total interstitial collagen volume density by 22% (from 5.5Ϯ3.8 Vv% to 4.3Ϯ3.2 Vv%, Pϭ0.04), whereas arteriolar wall area was slightly but not significantly reduced. Long-term therapy with the ACE inhibitor perindopril induces structural repair of coronary arterioles that is mainly characterized by the regression of periarteriolar fibrosis and associated with a marked improvement in coronary reserve. These findings indicate the beneficial reparative effects of ACE inhibition on coronary microcirculation in hypertensive heart disease. (Hypertension. 2000;36:220-225.) Key Words: arterioles Ⅲ collagen Ⅲ hypertension, arterial Ⅲ angiotensin-converting enzyme inhibitors Ⅲ coronary reserve A rterial hypertension is the most common cause of pressure overload of the left ventricle, and left ventricular (LV) hypertrophy (LVH) is its common sequelae. Furthermore, LVH is a strong independent risk factor for cardiovascular morbidity and mortality. 1 Potential mechanisms that might account for this observation include increased vulnerability of the hypertrophied myocardium to ischemic damage and enhanced arrhythmogenesis. 2 Moreover, it is increasingly recognized that patients with arterial hypertension and LVH have symptoms and signs of myocardial ischemia despite angiographically normal coronary arteries, and this was found to be related to impaired coronary flow reserve. 3 Functional and structural abnormalities of the coronary microcirculation have been described in hypertensive heart disease. 4 -6 Thus, an adequate increase in myocardial blood flow may be prevented in response to increased metabolic demand and may precipitate myocardial ischemia in these patients. 7 Important structural components of impaired coronary reserve are thickening of the media wall with reduced lumen size and accumulation of collagen in the periarteriolar region. 4,5 The thickening and hardening of arterioles have been called arteriolosclerosis and are characteristic of pathological hypertensive hypertrophy. 8,9 Antihypertensive treatment has been shown to normalize blood pressure and to reverse LVH in hypertensive patients...

show abstract

“…20 The reduced MBV in patients with HT is considered to indicate structural alterations within the hypertrophied heart. [7][8][9][10]21 Therefore, the determinants of MBV may overlap with the myocardial remodeling seen in the hypertensive heart with increased LVMI.…”

Section: Discussionmentioning

confidence: 99%

“…Important structural remodeling processes that lead to LVH are thickening of the medial wall of the small vessels with reduced lumen diameter and lowered density of coronary capillaries, as well as accumulation of extracellular matrix collagens in the perivascular region. [6][7][8][9][10] Angiotensinconverting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) have a regressive effect on the vascular changes in small coronary, renal, and cerebral arteries from animals with HT. 11,12 In patients with HT, a favorable effect of ACEIs and ARBs on the structure of subcutaneous small arteries has been reported.…”

mentioning

confidence: 99%

Angiotensin II Receptor Blocker, Valsartan, Increases Myocardial Blood Volume and Regresses Hypertrophy in Hypertensive Patients

Komatsu

Yamada

Iwano

et al. 2009

Circ J

View full text Add to dashboard Cite

eft ventricular hypertrophy (LVH) strongly predicts cardiovascular morbidity and mortality in patients with hypertension (HT). Rates of cardiovascular events have been reported as 2-to 4-fold higher in the presence of LVH in patients with HT, independent of standard risk factors. 1,2 Moreover, regression of hypertensive LVH is associated with improved prognosis, 3,4 so prevention or reversal of LVH in patients with HT is widely accepted as a desirable treatment goal.LVH associated with HT arises from hypertrophy of cardiac myocytes and extracellular matrix collagen deposition, 5 which stiffens the left ventricular (LV) and impairs diastolic filling. Important structural remodeling processes that lead to LVH are thickening of the medial wall of the small vessels with reduced lumen diameter and lowered density of coronary capillaries, as well as accumulation of extracellular matrix collagens in the perivascular region. 6-10 Angiotensinconverting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) have a regressive effect on the vascular changes in small coronary, renal, and cerebral arteries from animals with HT. 11,12 In patients with HT, a favorable effect of ACEIs and ARBs on the structure of subcutaneous small arteries has been reported. [13][14][15] However, these findings have been based on biopsies of subcutaneous tissue followed by dissection of small arteries or endomyocardial biopsies. The in vivo quantitative assessment of the myocardial microstructure thus remains to be studied in humans because of the lack of a suitable noninvasive technique.Recently, Vogel et al demonstrated that myocardial contrast echocardiography (MCE) could accurately measure the myocardial microvascular parameters, relative myocardial blood volume (MBV) and its exchange frequency (β). 16 Moreover, we have also reported a quantitative method of measuring MBV by harmonic power Doppler imaging during MCE, which can overcome the acoustic field inhomogeneity and correctly measure MBV in the diseased heart. 17 The MBV corresponds to the intravascular volume fraction and thus reflects the lumen diameter and density of capillaries, as well as perivascular fibrotic changes, within the region of interest (ROI). By using this technique, Indermuhle et al found that MBV was decreased in patients with HT. 18 However, it remains to be examined whether this decrease in MBV can be reversed by antihypertensive Sanae Kaga, BA**; Mutsumi Nishida, PhD**; Chikara Shimizu, MD**; Kazuhiko Matsuno, MD**; Hiroyuki Tsutsui, MD Background: Although a reduction in myocardial blood volume (MBV), an in vivo index of the myocardial microvasculature, measured by myocardial contrast echocardiography in patients with hypertension (HT), can be demonstrated, it is still unknown whether a decreased MBV can be improved by antihypertensive treatment. Methods and Results: Eleven HT patients (mean age 58 years, 7 men) with left ventricular hypertrophy (LVH) and 10 age-and sex-matched normal controls were studied. Harmonic power Doppler images were acqu...

show abstract

Structural analysis of arteriolar and myocardial remodelling in the subendocardial region of patients with hypertensive heart disease and hypertrophic cardiomyopathy

Cited by 60 publications

References 52 publications

Serum Carboxy-Terminal Propeptide of Procollagen Type I Is a Marker of Myocardial Fibrosis in Hypertensive Heart Disease

Serum Carboxy-Terminal Propeptide of Procollagen Type I Is a Marker of Myocardial Fibrosis in Hypertensive Heart Disease

Repair of Coronary Arterioles After Treatment With Perindopril in Hypertensive Heart Disease

Angiotensin II Receptor Blocker, Valsartan, Increases Myocardial Blood Volume and Regresses Hypertrophy in Hypertensive Patients

Contact Info

Product

Resources

About